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FEBS J. 2016 Jul;283(14):2653-60. doi: 10.1111/febs.13570. Epub 2015 Nov 6.

How does metabolism affect cell death in cancer?

Villa E1,2, Ricci JE1,2,3.

Author information

1
Inserm, U1065, Centre Méditerranéen de Médecine Moléculaire (C3M), équipe 'contrôle métabolique des morts cellulaires', Nice, France.
2
Faculté de Médecine, Université de Nice-Sophia-Antipolis, Nice, France.
3
Département d'Anesthésie Réanimation, Centre Hospitalier Universitaire de Nice, Nice, France.

Abstract

In cancer research, identifying a specificity of tumor cells compared with 'normal' proliferating cells for targeted therapy is often considered the Holy Grail for researchers and clinicians. Although diverse in origin, most cancer cells share characteristics including the ability to escape cell death mechanisms and the utilization of different methods of energy production. In the current paradigm, aerobic glycolysis is considered the central metabolic characteristic of cancer cells (Warburg effect). However, recent data indicate that cancer cells also show significant changes in other metabolic pathways. Indeed, it was recently suggested that Kreb's cycle, pentose phosphate pathway intermediates, and essential and nonessential amino acids have key roles. Renewed interest in the fact that cancer cells have to reprogram their metabolism in order to proliferate or resist treatment must take into consideration the ability of tumor cells to adapt their metabolism to the local microenvironment (low oxygen, low nutrients). This variety of metabolic sources might be either a strength, resulting in infinite possibilities for adaptation and increased ability to resist chemotherapy-induced death, or a weakness that could be targeted to kill cancer cells. Here, we discuss recent insights showing how energetic metabolism may regulate cell death and how this might be relevant for cancer treatment.

KEYWORDS:

Bcl-2 family; Warburg; cancer; cell death; chemotherapy; glucose; glutamine; metabolism; nonapoptotic death; oncogene

PMID:
26498911
DOI:
10.1111/febs.13570
[Indexed for MEDLINE]
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